Published Online
on November 10, 2005

A more recent version of this article appeared on December 1, 2005

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Submitted on July 28, 2005
Accepted on September 8, 2005

Neurogenesis in Rats After Focal Cerebral Ischemia is Enhanced by Indomethacin

Benjamin D. Hoehn PhD; Theo D. Palmer PhD; and Gary K. Steinberg MD, PhD^*

From the Department of Neurosurgery, Stanford University, Stanford, Calif.

^* To whom correspondence should be addressed. E-mail: gsteinberg{at}stanford.edu.

Background and Purpose--Newborn cells may participate in repair following ischemic brain injury, but their survival and function may be influenced by inflammation.

Methods--We investigated the effects of indomethacin, a nonsteroidal antiinflammatory drug, on the fate of newborn cells following transient focal ischemia.

Results--Bromodeoxyuridine (BrdU)-labeled cells, including migrating neuroblasts, were observed in the neighboring striatum and overlying cortex 1 day poststroke. The density of BrdU+ cells labeled with doublecortin, nestin, glial fibrillary acidic protein, or NG2 was increased at 14 and 28 days. Indomethacin increased BrdU+ cells of all lineages and reduced microglial/monocyte activation.

Conclusion--Indomethacin enhanced the accumulation of newborn cells following stroke.

Key words: brain infarction • brain ischemia • indomethacin • inflammation • ischemia • neurogenesis • stroke

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